In outpatient eating disorder treatment, non-compliance and premature interruption of therapy are affected primarily by factors which are related to patients' attitude and behaviour. These factors should be carefully addressed in patients with eating disorders to improve outcome.
Twenty-three chronic uremic patients on maintenance hemodialysis and suffering from severe pruritus were treated with activated powdered charcoal (6 g daily p.o.)· In 10 patients pruritus disappeared completely, and in 10 other patients a partial effect was observed. The favorable results persisted for several weeks after discontinuation of the treatment. Only 3 cases were totally unresponsive. No relevant undesirable side effects were observed with the exception of 1 case who showed treatment intolerance. It is concluded that activated charcoal per os is a safe, effective, and low-cost therapy for patients with uremic pruritus, but its mechanism of action is unknown.
In occasional cases of secondary hyperparathyroidism, long term stimulation of the parathyroid glands leads from compensatory to autonomous hyperfunction, and thus, hypercalcemia develops. This clinical entity, named tertiary hyperparathyroidism, is possibly due to the formation of an adenoma in one of the hyperplastic glands. Previous studies have shown that parathyroid adenomas may arise with allelic loss on chromosome 11. We tested for allelic loss at several loci on chromosome 11 in 12 enlarged parathyroid glands from 6 uremic patients and found loss of heterozygosity in 2 of the glands from 2 different patients with higher serum calcium levels (11.3 +/- 0.29 vs. 9.8 +/- 0.28 mg/dL; P< 0.004) and, therefore, ascribable to the so-called tertiary hyperparathyroidism. The 2 glands with allelic loss were significantly greater in mass than those without loss (3.42 +/- 0.37 vs. 1.60 +/- 0.54 g; P < 0.001). These data offer new evidence that autonomous parathyroid proliferation in uremic patients can develop through overgrowth by a monoclonal tumor, presumably with inactivation of a tumor suppressor gene(s) on chromosome 11.
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